from NEWSON ANDREW

1. MEDICAL SURGICAL NURSING
LOWER RESPIRATORY TRACT INFECTIONS
ENDOCARDITIS
BY NATIJUKA ANDREW
15/BSU/BNS/016

2. Endocarditis
• Endocarditis is inflammation of your heart’s inner
lining, called the endocardium. It’s usually caused
by bacteria.
• When the inflammation is caused by infection, the
condition is called infective endocarditis.
Endocarditis is uncommon in people with healthy
hearts.

3. Causes of endocarditis
• Streptoccocci(viridans)
• Staphylococci(aureus,epidermis,faecalis)
• Fungi(candida)
• Gram –ve bacteria(E.coli,klebsiella,pseudomonas)

4. s
• TRANSMISSION OF MICROORGANISMS
• brushing your teeth
• having poor oral hygiene or gum disease
• having a dental procedure that cuts your gums
• contracting a sexually transmitted disease
• using a contaminated needle
• through an indwelling urinary catheter or intravenous catheter

5. Risk factors for endocarditis
• injecting illicit intravenous drugs with a needle contaminated with
bacteria or fungi
• scarring caused by heart valve damage, which allows bacteria or germs to
grow
• tissue damage from having endocarditis in the pasthaving a heart defect
• having an artificial heart valve replacement

6. Distinction between Acute and Subacute Bacterial
Endocarditis
Feature Acute Subacute
Underlying Heart
Disease
Heart may be normal RHD,CHD, etc.
Organism S. aureus, Pneumococcus
S. pyogenes,
Enterococcus
viridans
Streptococci,
Entercoccus
Therapy Prompt, vigorous and initiated
on empirical ground
Can often be delayed
until culture reports and
susceptibilities
available

7. • z

10. Janeway Lesions

11. Splinter Hemorrhage

13. Subconjunctival Hemorrhages

14. Roth’s Spots

16. Treatment
• ATB therapy
• Surgery - performed in high-risk patients
• Age/comorbidities/PVE/DM
• Complicated IE (heart failure, shock…)
• High-risk agents (S.aureus, fungi…), ATB
failure
• TTE/TEE high-risk morphology parameters –
risk of embolisation

17. Antibiotics
• beta-lactam (penicillin, cefalosporin)
• glykopeptide (vancomycine)
• aminoglykosides (gentamicin)
• rifampicin in PVE
Fungi – ATB centre expert consult

18. Antibiotics
• Streptococci: PEN/CEF + GENTA, (VANCO)
• Enterococci: like streptococci, PEN resist. common
• Staphylococci: MET/OXA + GENTA
• Empiric therapy - should focus on S. aureus
• HACEK/early PVE/fungi - require expert ATB consult
• PVE - prolonged (min. 6w) + RIFAMPIN

19. Antibiotics
• Usually 4-6 weeks (regardless of surgery)
• No fever and decrease in CRP are good markers
of th. success, TTE follow-up (< 2weeks) necessary
• Cessation of therapy in case of:
• normal CRP (1w), favourable TTE, no
embolisation (2w), absence of focus for
potential reinfection

20. Surgery
• progressive heart failure (emergency in shock)
• signs of ATB th. failure - continuous fever,
abscess, vegetation, valve dehiscence…
• embolization potential (> 10 mm)

21. NURSING MANAGEMENT
• NURSING ASSESSMENT
• Shortness of breath
• Stabbing chest pain
• Decreased ability to exercise
• Irregular heartbeat
• Dyspnea
• Body swelling
• Palpitations

22. NURSING CARE PLAN
DIAGNOSIS GOAL INTERVATION RATIONALE EVALUATION

23. NURSING DIAGNOSIS
•
1. Acute pain related to systemic effects of infection.
Interventions :
Independent
 Assess the complaint of chest pain. Pay attention to nonverbal cues of discomfort.
 Provide a quiet environment and comfort measures, such as: changes in position, back
rub, use a warm compress / cold.
 Give proper entertainment activities.
• Collaboration
 Give medications as indicated.
 Give O2 supplementation as indicated.
•

24. • Rationale :
 Chest pain may and may not accompany the presence or absence
of ischemia depends endocarditis.
 This action can reduce the patient's physical and emotional
discomfort.
 Redirecting attention, provide distraction in the level of individual
activities.
 Can relieve pain, decrease the inflammatory response.
 Maximize the availability of O2 to reduce the workload of the heart
and prevent ischemia.
•

25. • 2. Risk for decreased cardiac output related to disorders of the heart valves and the endothelium.
Interventions :
Independent
 Monitor frequency / rhythm, heart sounds.
 Provide comfort measures, for example; back rub, semi-Fowler's position and entertainment.
• Collaboration
 Give medications as indicated.
• Rationale :
 Tachycardia and distritmia can occur when the heart is working to increase, rising to fever, hypoxia
and ischemia.
 Increase relaxation and redirecting attention.
 Increase ventricular contraction.
•

26. • 3. Altered body temperature related to the infection process.
Interventions :
Independent
 Assess for dehydration, diaphoresis, poor skin turgor, dry mucous membranes.
 Measure the body temperature 4-8 hours.
 Monitor the input and output of fluids every 8 hours.
 Monitor the IV presence of redness and swelling, change places every 24 hours.
• Collaboration
 Give antibiotics antipyretic to order, make sure the drug is administered according to the time.
• Rationale:
 Increased heat causes the discharge through evaporation.
 Further support the diagnosis.
 Knowing the fluid balance while an increase in temperature.
 Prevent the occurrence of phlebitis.
•

27. • 4. Risk for Ineffective tissue perfusion related to embolization
Interventions :
Independent
 Assess for signs of embolization, report any signs of embolization to the doctor immediately.
 Perform a neurological examination or according client's condition.
 Instruct the client about the need to continue anticoagulation, if ordered for further prevent embolic
period.
 Encourage active with range of motion exercises as tolerated.
• Collaboration
 Give anticoagulant therapy.
• Rationale
 The presence of emboli causing blockage of blood flow resulting in tissue hypoxia.
 Help enforce the subsequent diagnosis.
 Reduce the formation of embolism due to freezing blood cells.
 Improves peripheral circulation and venous return to reduce thrombus formation and embolism.
•

28. EVALUATION
• 1. Acute pain related to systemic effects of infection.
 Reported pain gone / controlled.
 Demonstrate the use of the skills of relaxation and diversion
activities as indicated for individual situation.
 Identify methods that give disappearance.
•

29. • 2. Risk for decreased cardiac output related to disorders of the heart valves and the
endothelium.
 Nutritional status is maintained / repaired.
 Achievement fixes weight according to age, gender.
 Clients revealed increased appetite.
•
3. Altered body temperature related to the infection process.
 Inflammatory process has been lost.
 Moist and dry skin.
• 4. Risk for Ineffective tissue perfusion related to embolization
 Cerebral tissue perfusion is maintained.
 Clients conscious and oriented.
 No signs of embolization.
•

30. Myocarditis

31. Overview
• Inflammatory disease of the myocardium with a
wide range of clinical presentations, from subtle
to devastating
• Usually manifests in otherwise healthy person
• Wide variety of infectious organisms,
autoimmune disorders and exogenous agents
• Acute phase (0-2wks): direct cytotoxic effect +
cell mediated cytotoxicity
• Chronic phase (>2wks): mainly autoimmune

32. Etiology
• “Idiopathic” in 50% of cases
• Viruses - Enterovirus, Coxsackie A,B, Adenovirus,
Parvovirus B19, Influenza, CMV,EBV, HCV, HIV…
• Bacterial - streptococci, TBC, diptheria, Borrelia,
Chlamydia, Mycoplasma
• Fungi – Aspergillus, Candida
• Protozoa – Trypanosoma cruzii
• Drugs - anthracyclines, cocaine
• Rheumatic fever
• Autoimmune disorders – SLE, Sarcoidosis, Sjögren
sy, Churg-Strauss sy, Wegeners granulomatosis,
„giant-cell“ myocarditis

33. Clinical presentation
• flu-like symptomes, arthralgias, malaise, fever
• pharyngitis, tonsillitis, upper respiratory tract
infection
• Chest pain, sweats, dyspnea, palpitations
• Signs of heart failure, cardiogenic shock
• Syncope or sudden cardiac death due to underlying
ventricular arrhythmias or AV block)

34. Diagnostic workup
• Complete blood count, erythrocyte
sedimentation rate level, CRP, rheumatologic
screening, cardiac biomarkers (TnI, TnT)
• Viral antibody titers - rarely indicated, low
specificity and delayed rising, no impact on
therapeutic decisions
• ECG - nonspecific - sinus tachycardia, ST-T
changes, AV blocks
• Echocardiography (TTE) - to estimate
dysfunction and rule-out other causes

35. Diagnostic workup
• CAG (coronary angiography)- rule-out CAD
• MRI (late gadolinium enhancement) - extent
of inflammation and cellular edema, nonspecific
• EMB (endomyocardial biopsy) - routine use
rarely helpful, mandatory in rapidly progressive
HF to rule-out giant-cell myocarditis

36. Medical management
• ANTIBIOTIC THERAPY(PRP+GETAMICIN,Vancomycin+Gentamicim)
• Cardiotonic drugs(digitalis+related drugs)
• Restrict sodium diet
• Heart transplant in severe cardiomyopathy.

37. NURSING MANAGEMENT(CARE PLAN)
DIAGNOSIS GOAL INTERVATION RATIONALE EVALUATION

38. Pericarditis

39. Pericardial physiology
• Parietal layer
• Thick, collagenous, stiff
• Adventitial attachments to sternum, diaphragm, mediastinum
• Visceral layer
• Thin
• Closely adherent to epicardial surface

40. Pericardial fluid
• Potential space between layers
• Normally 15-60 cc fluid
• Functions
• Reduces friction
• Prevention of infection
• Augmentation of atrial filling
• Maintains normal pressure-volume relationship of
chambers
• No physiological consequence to absent
pericardium

41. Pericardial innervation
• Parasympathetic
• Vagus
• Left-recurrent laryngeal nerve
• Sympathetic
• Stellate
• First thoracic ganglia
• Little somatic sensory innvervation
• Thus visceral nature of chest pain

42. Pericarditis - etiology
• Viral
• Bacterial
• Traumatic
• Malignant
• Post-irradiation
• Post-MI
• Drug-induced
• Collagen vascular disease

43. Viral Pericarditis
• Most common cause
• Enteroviruses
• Coxsackie A & B
• Echovirus
• HIV
• Mechanism of injury
• Direct viral cytotoxicity
• Indirect auto-antibody mediated effects

44. Viral Pericarditis - SSx
• Syndrome may be immediate or develop 2-4
weeks post viral illness
• Chest pain
• Pericardial friction rub
• Heard with diaphragm over LLSB, leaning forward, breath held
• Scratchy
• Triphasic (presystolic, systolic, diastolic)
• Fever
• Tachycardia
• Tachypnea,dyspnea
• diaphoresis

45. Bacterial Pericarditis
• Common in less developed countries
• More commonly associated with tamonade
• Higher mortality than viral
• Streptococcus, staphylococcus, gram negs, anaerobes
• TB
• Lyme disease

46. • Concomitant pneumonia / empyema
• Often not diagnosed until tamponade
• Definitive Dx requires pericardiocentesis
• Treatment Abx
• ICU admission indicated

47. Uremic Pericarditis
• ESRD / Underdialysis
• Bloody pericardial effusions
• ECG often normal (little epicardial involvement)
• Cardiac tamponade common
• Often loculated - therapeutic pericardiocentesis difficult
• Treatment
• ICU admission
• NSAIDS (caution b/c bleeding diathesis of uremia)

48. Post-MI Pericarditis
• May occur within days of MI
• Direct extension of myocardial inflammation
• Presents as “different” chest pain
• Must distinguish from reinfarction
• Incidence 7-16%
• Tx: NSAIDs
• Dressler’s syndrome
• Thought to be autoimmune
• Weeks to months
• Fever, chest pain, leukocytosis, pleuritis,
pericardial/pleural effusions
• Tx: NSAIDs, steroids for resistant cases

49. Collagen Vascular Disease Pericarditis
• Common in many CVDs
• RA
• Incidence 30-50% - many clinically silent
• SLE
• 50% incidence
• Dx: CP, R CHF, echo
• ECG/CXR often normal
• Tx: steroids
• Commonly progress to constrictive pericarditis

50. Malignant pericarditis
• Primary tumours rare
• Metastatic disease common
• Incidence 10% in cancer patients
• Lung, breast, lymphoma, leukemia, MM
• Children – Hodgkin’s, leukemia, lymphosarcoma
• Progress to tamponade in 50-85%
• Dx: pericardiocentesis / cytology
• Tx: symptomatic

51. Post-Irradiation Pericarditis
• Early (days – months)
• Dose related pericardial effusion
• Must distinguish from malignant effusion
• SSx:
• SOBOE
• can mimic infectious pericarditis (fever, CP, friction rub)
• Tx:
• Often resolves spontaneously
• NSAIDs, steroids, pericardiocentesis
• Late (years)
• Constrictive pericarditis
• Tx:
• Often requires pericardiectomy

52. • SLE-like syndrome
• Procainamide
• Hydralazine
• Isoniazid
• Methyldopa
• Reserpine
• Hypersensitivity
reaction
• Penicillin
• Cromolyn sodium
• Methysergide
• constrictive pericarditis /
generalized mediastinal
fibrosis
• Doxorubicin
• Chemotherapy
• Pericarditis /
cardiomyopathy
Drug-induced pericarditis

53. Pericardial Disease
• Pericarditis
• Non-specific inflammation of pericardium
• Rarely emergent
• Pericardial effusion
• Accumulation of fluid in pericardial space
• Serous, purulent, fibrinous, hemorrhagic
• Cardiac tamponade
• Impairment of ventricular filling due to fluid in
pericardial space
• Emergent

54. pericarditiscomplications

55. Pericardial Effusion
• Collection of fluid in indistensible pericardium
• Secondary to pericarditis
• infectious, uremic, malignant, post irradiation
• Secondary to hemorrhage / trauma
• aortic dissection, penetrating trauma
• Symptoms related to size and acuity of collection
• 80-100cc required before decompensation begins (15-
60cc fluid normal)
• Chronic effusions rarely progress to tamponade

56. Pericardial tamponade
• Physiologic decompensation due to pericardial
effusion
• Acute surgical tamponade
• Penetrating injury
• aortic dissection
• Iatrogenic (central line insertion)
• Medical tamponade
• Due to pericardial effusions due to pericarditis
• Low-pressure tamponade
• Due to severe dehydration
• LV pressure lowered to equilibrate with RV pressure

57. Pericardial tamponade
• Early
• <200cc,  CVP, tachycardia
• Moderate
• ~200cc,  CVP, tachycardia,  cardiac output,  BP
• Severe
• >200cc,  CVP (unless hypovolemic),  BP,  
cardiac output, +/- bradycardia

58. Traumatic Tamponade
• 2% of penetrating thoracic trauma
• 80-90% of stab wounds to heart
• 20% of GSW to heart
• Large instruments cause exsanguination
• Foreign bodies, rib fractures
• Iatrogenic – cardiac catheterization, pacemaker
insertion, pericardiocentesis, cardiac surgery

59. Clinical presentation
• Intermittent fever
• dyspnea/tachypnea (!myocarditis, pericarditis,
and cardiac tamponade)
• cough, dysphagia
• Any form of pericardial inflammation may
cause effusion
Myocarditis ↔ myopericarditis
Pericarditis ↔ perimyocarditis

60. Etiology
• Idiopathic causes - about 50%, likely viral
• Infectious
• Viral – enterovirus,echovirus, parvovirus, EBV, HIV…
• bacterial, TBC, mycotic (Candida)
• Inflammatory disorders - RA, SLE, scleroderma,
rheumatic fever, Reiter sy, dermatomyositis
• Metabolic – renal failure, hypothyroidism,
• Cardiovascular disorders - acute MI, Dressler syndrome,
• Iatrogenic – postpericardiotomic sy, catheterization
• Neoplasms – adjacent / secondary / paraneoplastic
• Drugs, Irradiation
• Trauma, Pneumonia, Pulmonary infarction…

61. Clinical features
• Beck’s triad:
• hypotension
• distended neck veins (>15mm H20 with hypotension is
diagnostic)
• muffled heart sounds (unlikely to be heard in trauma
room)
• pulsus paradoxus – difficult to measure during
resuscitation
• no response to vigorous fluid resuscitation

62. Diagnostic workup
• ECG changes
• chest radiograph (enlarged if effusion >250ml)
• TTE (effusion), CT (calcification), MRI
• Laboratory studies (Complete blood count, ESR,
CRP, cardiac TnI/TnT, electrolytes, BUN, creatinine,
thyroid hormones + specific (RF...))
• CAG ?

63. ECG – ECG vs Pericarditis
Pericarditis Ischemia/Infarction
ST elevation Diffuse, concave Anatomical, convex
ST changes few reciprocal
changes
Reciprocal changes
PR segment Depression No depression
Q-T
prolongation
Rarely without
myocarditis
More commonly seen
Evolution Normalization in
stage 2
MI progression with
development of Q-
waves
Electrical
Alternans
Present with
tamponade
absent

66. Treatment
• If specific cause revealed, treat accordingly (ATB)
• Idiopathic or viral treated for symptom relief
• NSAIDs in full dose for 7-14 days (600-800 mg
ibuprofen /day), consider PPI as gastric
protection
• Colchicine (recurrence or beyond 14 days, 1
mg/day)
• Corticosteroids - not for initial therapy, unless
specific therapy (autoimmune) or no response to
NSAIDs + colchicine
• Pericardiocentesis – large effusions, cardiac
tamponade

67. Management
• Emergency Department
• vigorous fluid resuscitation
• CVP monitoring
• Treat concomitant injuries
• Pericardiocentesis
• ED thoracotomy

68. Pericardiocentesis

69. Pericardiocentesis
• Diagnostic and therapeutic
• Many false positives / false negatives (clotted blood)
• Improvement possible with small volume of blood removed
• Complications
• Pericardial tamponade
• Laceration of coronary artery / lung
• Induction of dysrhythmia
• Continued deterioration may necessitate thoracotomy

70. Pericardiocentesis
• Technique
• 18 gauge, 10 cm spinal needle, 20 cc syringe
• Continuous ECG monitoring
• Needle enters subxyphoid area
• Aim for left scapula
• Aspirate every 1-2 mm
• Stop if blood aspirated, cardiac pulsations felt, ECG
changes
• NB: if more than 20 cc blood is removed easily you are
probably in the RV (ooops!)

71. NURSING MANAGEMENT(CAREPLAN)
DIAGNOSIS GOAL INTERVATION RATIONALE EVALUATION

72. Thank You.